FGF-23 is elevated by chronic hyperphosphatemia

A. Gupta, K. Winer, M. J. Econs, S. J. Marx, M. T. Collins

Research output: Contribution to journalArticle

123 Citations (Scopus)

Abstract

The identification and characterization of FGF-23 has provided an opportunity to gain new insight into phosphorus metabolism. Circulating FGF-23 promotes renal excretion of phosphorus, and FGF-23 is measurable in the serum of normal subjects. Serum levels of FGF-23 are elevated in patients with renal phosphate wasting disorders such as tumor induced osteomalacia, X-linked hypophosphatemia and fibrous dysplasia. However, the factors that alter its serum concentration are not known. The study of serum FGF-23 is confounded by the fact that high serum calcium, PTH, and any other putative phosphotonins, have similar effects on serum and urine phosphorus. To circumvent the confounding effect of serum PTH and calcium, we studied serum FGF-23 and phosphate levels in patients with chronic hypoparathyroidism and hyperphosphatemia. Serum was collected in the morning after an overnight fast from three groups: 1) 9 patients with chronic hypoparathyroidism on stable treatment with calcium and calcitriol, 2) 9 patients with primary hyperparathyroidism, and 3) 77 normal controls. Patients with hypoparathyroidism had predictably higher levels of serum phosphorus than patients with hyperparathyroidism or normal controls (5.6± 1.1, 3.1± 0.6, and 3.1± 0.5 mg/dL, mean ± 1 SD, respectively (p<.0.01 for hypoparathyroid vs: either group)). They also had higher levels of FGF-23 (150±120 vs: 70±60, or 55±20 RIU/ml, respectively (p<0.05 vs: either group)). In conclusion, serum FGF-23 levels are elevated in patients with hyperphosphatemia and chronic hypoparathyroidism, suggesting a feedback system in which serum FGF-23 responds to serum phosphorus and regulates it. However, in the setting of chronic hypoparathyroidism, the degree of elevation of FGF-23 is insufficient to normalize serum phosphorus.

Original languageEnglish (US)
Pages (from-to)4489-4492
Number of pages4
JournalJournal of Clinical Endocrinology and Metabolism
Volume89
Issue number9
DOIs
StatePublished - Sep 1 2004

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Hyperphosphatemia
Phosphorus
Serum
Hypoparathyroidism
Calcium
Phosphates
Calcitriol
Metabolism
Tumors
Feedback
Familial Hypophosphatemic Rickets
Primary Hyperparathyroidism
Hyperparathyroidism

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

FGF-23 is elevated by chronic hyperphosphatemia. / Gupta, A.; Winer, K.; Econs, M. J.; Marx, S. J.; Collins, M. T.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 89, No. 9, 01.09.2004, p. 4489-4492.

Research output: Contribution to journalArticle

Gupta, A. ; Winer, K. ; Econs, M. J. ; Marx, S. J. ; Collins, M. T. / FGF-23 is elevated by chronic hyperphosphatemia. In: Journal of Clinical Endocrinology and Metabolism. 2004 ; Vol. 89, No. 9. pp. 4489-4492.
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AB - The identification and characterization of FGF-23 has provided an opportunity to gain new insight into phosphorus metabolism. Circulating FGF-23 promotes renal excretion of phosphorus, and FGF-23 is measurable in the serum of normal subjects. Serum levels of FGF-23 are elevated in patients with renal phosphate wasting disorders such as tumor induced osteomalacia, X-linked hypophosphatemia and fibrous dysplasia. However, the factors that alter its serum concentration are not known. The study of serum FGF-23 is confounded by the fact that high serum calcium, PTH, and any other putative phosphotonins, have similar effects on serum and urine phosphorus. To circumvent the confounding effect of serum PTH and calcium, we studied serum FGF-23 and phosphate levels in patients with chronic hypoparathyroidism and hyperphosphatemia. Serum was collected in the morning after an overnight fast from three groups: 1) 9 patients with chronic hypoparathyroidism on stable treatment with calcium and calcitriol, 2) 9 patients with primary hyperparathyroidism, and 3) 77 normal controls. Patients with hypoparathyroidism had predictably higher levels of serum phosphorus than patients with hyperparathyroidism or normal controls (5.6± 1.1, 3.1± 0.6, and 3.1± 0.5 mg/dL, mean ± 1 SD, respectively (p<.0.01 for hypoparathyroid vs: either group)). They also had higher levels of FGF-23 (150±120 vs: 70±60, or 55±20 RIU/ml, respectively (p<0.05 vs: either group)). In conclusion, serum FGF-23 levels are elevated in patients with hyperphosphatemia and chronic hypoparathyroidism, suggesting a feedback system in which serum FGF-23 responds to serum phosphorus and regulates it. However, in the setting of chronic hypoparathyroidism, the degree of elevation of FGF-23 is insufficient to normalize serum phosphorus.

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